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Dawn's picture

Inferior Posterior M.I.

This is a "classic" ECG of very good quality for you to use in a classroom setting.

The Patient:  A 57-year-old man who complains of a sudden onset of "sharp" chest pain while on a long bike ride.  The pain does not radiate, and nothing makes it worse or better.  He is pale, cool, and diaphoretic.  His medical history is unknown.

The ECG:  This ECG could be considered "classic" for an inferior wall ST elevation M.I. caused by occlusion of the right coronary artery.  ECG findings include:

*   Normal sinus rhythm

*   Marked ST elevation in Leads II, III, and aVF.  The elevation is higher in Lead III than in Lead II, a reliable sign of RCA occlusion.

*   Reciprocal depression in Leads aVL and I.  ST depression in the setting of acute transmural ischemia (STEMI) is almost ALWAYS due to  reciprocal change. The fact that this STD is localized to leads that are reciprocal to the inferior wall is proof of the nature of the STD.

*   Reciprocal depression in V1 - V3.  More localized depression.  What wall is reciprocal to the anterior-septal wall?  The posterior (postero-lateral).  Since the inferior wall is really the lower part of the posterior wall, inferior wall M.I. is often accompanied by posterior wall M.I.

An additional lead, V4R, is helpful in this situation, since the right ventricle is often affected in RCA occlusions.  The EMS crew reports that V4R was negative for ST elevation, but we do not have a copy.

Small q waves have formed in Lead III, and we would watch for progression of this sign, as it can indicate necrosis.

Outcome:  The patient went to the cath lab, but we have no further followup.


Our thanks to Ashley Terrana for donating this tracing.



Dawn's picture

Large Anterior Wall M.I. and Effect of Lead Reversal

EDIT: Please refer to the comments below this text. The second ECG in this series shows unexpected QRS and ST-T morphology changes, which I tried to explain by way of the patient's long anterior descending coronary artery. However, Dave Richley, who is a very well-known cardiac physiologist and ECG Guru took the time to analyze these morphologies and realize they can be explained by an inadvertent ECG LEAD MISPLACEMENT. This patient does have a proximal lesion of the LAD, proven and repaired in the cath lab. But the inferior wall does not have the injury it appears to have in this second ECG. Thanks to Dave for reminding us to slow down and look closely when things don't look "right".

The Patient:   These two ECGs, taken 26 minutes apart, were obtained from a 50-year-old man who complained of sudden onset of chest pain.  He denied history of coronary artery disease. He was Covid-positive, and the rest of his medical history was unremarkable.

ECG No. 1:  This ECG was obtained by paramedics enroute to the hospital.  For your beginner-level students, it will be easy to demonstrate the large ST elevations in V3 through V6. The machine’s measurements at the bottom confirm that this ECG meets any field criteria for ST elevation M.I. “STEMI”.

But there is so much more to see! Taking a methodical approach, and starting with rate and rhythm, we see sinus bradycardia at 57 bpm. Intervals and frontal plane axis are within normal limits. R wave progression in the chest leads is stalled in V1- V3 due to loss of initial r waves (narrow QS). The transition to positive deflections in V4 – V6 is abrupt.  These q waves in the V1 and V2 appear narrow, but V3 appears to have a Q wave that is almost wide enough to be considered pathological.  Narrow Q waves may be a transient sign of injury, while wide ones (>40 ms) are an ECG sign of necrosis.

Dawn's picture

Inferior Wall M.I. With Wide QRS and Complete AV Block

This ECG is from a 66-year-old woman who called 911 for a complaint of chest pain for the past four hours. She also complained of nausea, vomiting, and diarrhea for that time. She was pale and diaphoretic, and her BP was 77/43 sitting up, improving to 90/54 reclining. She denied “cardiac” history.  Her medications included:  aspirin, an SSRI, cilostazol, amlodipine, umeclidinium and vilanterol inhaler, atorvastatin, levothyroid, and metoprolol. We don’t have a previous ECG.  The EMS crew followed their chest pain protocol and delivered the patient to a facility with an interventional cath lab, but they did not designate a “STEMI Alert” because of the wide QRS.  It is their protocol to use the term “STEMI Alert” only when no M.I. mimics, such as left bundle branch block, are present. 

What does this ECG show?     There is an underlying sinus rhythm at 75 bpm.  There is AV dissociation, with regular, wide QRS complexes at a rate of 44 bpm.   This meets the criteria for complete heart block (third-degree AV block).  The morphology of the QRS complexes meets the criteria for left bundle branch block (wide, upright in Leads I and V6, negative in V1).  At a rate of 44 bpm, several options for this escape rhythm are possible:  1)  junctional escape with LBBB, 2) junctional escape with intraventricular conduction delay due to AMI,  and 3) idioventricular escape rhythm.   Also, in the presence of IWMI, AV node ischemia is very likely, resulting in AV blocks at the level of the AV node.  CHB at the AV node would result in junctional escape rhythm, and CHB below that, in the fascicles of the bundle branches, would result in idioventricular escape. The issue for this patient, and ANY patient, is cardiac output, and we see several reasons for cardiac output to be lower:

·         Wide QRS

Dawn's picture

Inferior Wall M.I.

This ECG shows a common manifestation with inferior wall M.I., BRADYCARDIA.  We see the signs of acute inferior wall M.I. in the inferior leads:  II, III, and aVF all have ST segment elevation.  There almost appear to be pathological Q waves in Leads III and aVF.  There are still VERY tiny r waves, and the downward deflections are not wide, but should full-blown Q waves develop in these leads, they would signify necrosis in the area.  A repeat ECG would certainly be warranted. 

Another sign that there is an inferior wall STEMI is the ST segment depression in Leads I and aVL, which are reciprocal to Lead III.  ST depression can have many meanings, but when it is localized in the leads which are opposite ST elevation, it is reciprocal.  There is also ST depression in Leads V1 and V2.  These leads are reciprocal to the POSTERIOR wall, otherwise known as the upper part of the inferior wall.  If an inferior wall M.I. is large enough, it can produce ST elevation in the posterior leads (not performed in this case), and ST depression in the anterior leads, especially V1, V2, and V3. 

The rhythm is a marked sinus bradycardia, at just under 40 beats per minute.  Sinus bradycardia is very common in inferior wall M.I., because the inferior wall and the sinus node are usually both supplied by the right coronary artery.  AV blocks can also occur because the AV node is also supplied by the RCA in most people. 

It is important to remember that bradycardia does not always need to be treated.  In patients with acute M.I., a well-tolerated bradycardia may actually be beneficial to the injured heart, reducing supply/demand ischemia.  A well-tolerated bradycardia is a rate that does not produce low blood pressure and poor peripheral perfusion.  Some people tolerate rates in the 40’s quite well.  If the patient shows signs of poor perfusion: low BP, decreased mentation, pallor, shortness of breath, the rate should be cautiously increased with medication or electronic pacing.  


Dawn's picture

Inferior Wall M.I. and Right Bundle Branch Block

This ECG shows two obvious abnormalities, right bundle branch block AND inferior wall M.I.  It is also a good teaching example of how the terminal wave of RBBB can be mistaken for the ST elevation of M.I.

First, check this ECG to see if it meets the criteria for right bundle branch block:

1)  The QRS will be wide. That is, it will be greater than or equal to .12 seconds (120 ms).  In this case, the QRS is 134 ms.

2)  The rhythm will be supraventricular.  Supraventricular rhythms originate from above the ventricles.  This ECG has P waves before each QRS.  Even though the rhythm is irregular, slowing down during this recorded period, it is a sinus rhythm.

3)  The QRS will have a terminal wave after the "normal" part of the QRS.  This represents the right ventricle depolarizing late.  It is very easily seen in V1, which normally has an rS pattern, and with RBBB has an rSR' pattern, making it appear upright.  V6 and Lead I will show this terminal wave as a wide little s wave.

As mentioned, there is also an acute inferior wall M.I. here.  The ST segment elevation in Leads II, III, and aVF are actually quite subtle.  The flat top of the ST segments gives them away as abnormal, along with the associated ST elevations in V5 and V6, and the reciprocal ST depressions in V1 through V3.  Normally, in IWMI, there will be reciprocal ST depressions in Leads I and aVL, but the elevations they are reflecting are very subtle, and so, therefore, are the depressions. 

The tricky thing about this ECG is that you must look carefully at the inferior wall leads to see the true ST elevation, which, as mentioned, is subtle.  The RBBB terminal wave of the QRS complexes in Leads III and aVF is upright, and is often mistaken for ST elevation.  Remember, ST segments are smooth from the end of the QRS to the peak of the T wave.  See the detail illustration.

This ECG is suitable for your classes from beginner level (rate variation in sinus rhythm) through advanced (clinical significance of RBBB in acute M.I.).  It also offers an example of reciprocal ST changes, and of a situation where the inferior leads II, III, and aVF are related to the low lateral leads V5 and V6 by a shared blood supply.

Dawn's picture

Inferior Wall MI With Artifact

This ECG is taken from a 66-year-old man who presented to the Emergency Dept. with a complaint of chest pain.  The ECG shows clear signs of acute inferior wall MI:  ST segment elevation in Leads II, III, and aVF and reciprocal ST depression in Leads I and aVL.  In addition, there are reciprocal ST depressions in Leads V1, V2, and V3.  These indicate that the MI extends up the inferior wall into the area called by most clinicians the posterior wall.  When the injured area extends high enough from the inferior wall, it becomes visible to the anterior-septal leads as ST depression.  There is also a small ST elevation in Leads V5 and V6, the low lateral wall, indicating a common blood supply for the inferior and low lateral walls (usually the right coronary artery).  All of these findings make this a rather "typical" inferior wall MI.

Unfortunately, this ECG also has a significant amount of artifact.  The second, sixth, and tenth "beats"  appear to be  premature beats in Leads I and II.  However, it is important to remember that the four channels on this ECG are run simultaneously.  That is, any complex of significant voltage should show up four times.  The "premature" beats do not appear in Lead III, and do not affect the timing of the appearance of the next beat at all.  They also appear during moments of baseline disruption, indicating that they are not heartbeats, but simply artifact.

Why is this important?  Artifact makes the ECG hard to interpret accurately.  The ECG machine even had a difficult time, completely ignoring obvious P waves, and calling the rhythm "atrial fibrillation".  Every effort should be made to obtain the cleanest, most artifact-free ECG possible.

Additional note:  it can be very informative to do a right-sided ECG on an IWMI patient, or at least a V4Rt.  In fact, it is a protocol requirement in many EMS agencies.  Right ventricular infarction can change the hemodynamics of your patient, causing a need for fluid resuscitation. In fact, a drop in BP, such as that caused by nitroglycerin, can cause circulatory collapse.  Ntg should be given cautiously to RVMI patients.  Fortunately, IV fluids will seldom cause left heart overload in these patients.  A look at the right ventricle with V4Rt can be very helpful in deciding treatment options.

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